Editing Sepsis/SIRS (section)

=== '''Normal response to infection''' ===

** Host response initiated when innate immune cells (especially macrophages) recognise and to microbial components
*** Pattern-recognition receptors (PRRs) on the surface of immune cells recognise and bind to microbial pathogen-associated molecular patterns (PAMPs) or endogenous danger signals
**** PRRs include toll-like receptors (TLRs) and others
*** Neutrophils begin to defend against pathogens - phagocytosis, secretion of antimicrobial peptides, and the release of neutrophil extracellular traps (NETs)
*** Signalling cascade developed via the activation of cytosolic nuclear factor-kb (NF-kb), which leads to activation of genes involved in host inflammatory response such as TNF-a, IL-1, IL-6, chemokines, vascular adhesion molecule-1, and nitric oxide
*** Polymorphonuclear leucocytes become activated and aggregate at site of infection, causing warmth and erythema due to local vasodilation and hyperaemia
*** Pro-coagulant status causes micro-thrombosis
*** Some anti-inflammatory mediators balance this activation
*** If the inflammatory process is balanced, haemostasis is restored, leading to tissue repair and healing